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 Blood, 1 March 2008, Vol. 111, No. 5, pp. 2674-2680.
Prepublished online as a Blood First Edition Paper on January 7, 2008; DOI 10.1182/blood-2007-08-110205.

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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY

Semaphorin 3A suppresses VEGF-mediated angiogenesis yet acts as a vascular permeability factor

Lisette M. Acevedo1, Samuel Barillas1, Sara M. Weis1, Joachim R. Göthert2, and David A. Cheresh1

1 Department of Pathology and Moores UCSD Cancer Center, University of California, San Diego, La Jolla; and 2 Department of Hematology, University Hospital, Essen, Germany

Semaphorin 3A (Sema3A), a known inhibitor of axonal sprouting, also alters vascular patterning. Here we show that Sema3A selectively interferes with VEGF- but not bFGF-induced angiogenesis in vivo. Consistent with this, Sema3A disrupted VEGF- but not bFGF-mediated endothelial cell signaling to FAK and Src, key mediators of integrin and growth factor signaling; however, signaling to ERK by either growth factor was unperturbed. Since VEGF is also a vascular permeability (VP) factor, we examined the role of Sema3A on VEGF-mediated VP in mice. Surprisingly, Sema3A not only stimulated VEGF-mediated VP but also potently induced VP in the absence of VEGF. Sema3A-mediated VP was inhibited either in adult mice expressing a conditional deletion of endothelial neuropilin-1 (Nrp-1) or in wild-type mice systemically treated with a function-blocking Nrp-1 antibody. While both Sema3A- and VEGF-induced VP was Nrp-1 dependent, they use distinct downstream effectors since VEGF- but not Sema3A-induced VP required Src kinase signaling. These findings define a novel role for Sema3A both as a selective inhibitor of VEGF-mediated angiogenesis and a potent inducer of VP.


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